Figure 6
Figure 6. Influence of CD1d on hematopoietic stem cells. Comparative engrafting capacities of WT control and CD1d−/− HSCs in lethally irradiated primary mice in a competitive transplantation setting (A,B,D) and a noncompetitive setting (C) without (A-C) and with (D) pretreatment of donor cells with anti-CD1d Ab. All secondary recipient transplantations were done in a noncompetitive setting. Results are expressed as CD45.2+ cell chimerism shown as mean ± SEM with significant differences from WT or untreated cells noted and are based on individual analysis of BM from 3 WT or 3 CD1d−/− mice, each injected intravenously into 5 lethally irradiated recipient B6.BoyJ (CD45.1+) mice along with 5 × 105 nonirradiated B6.BoyJ competitor cells for a total of 15 recipient mice/group (A and B). For secondary transplantations (noncompetitive situation), cells from 9 primary recipients of each group (WT or CD1d−/−) were each injected into 3 lethally irradiated B6.BoyJ mice for a total of 27 recipients per group (A and B). For panel C, 5 × 105 WT or CD1d−/− cells were transplanted as noted in panels A and B in primary B6.BoyJ recipients and secondary transplantations. For panel D, results of CD45.2+ cell chimerism (mean ± SEM) are shown with significant differences noted compared with isotype control Ab–treated cells. 10 × 106 CD45.2+ BM cells were treated with Ab for 30 minutes at 4°C, washed, and injected intravenously at a 1:1 donor-to-nonirradiated (B6.BoyJ, CD45.1+) competitor cell ratio into lethally irradiated B6.BoyJ mice for engraftment analysis of primary mice. Treated donor cells from 3 mice/group were each transplanted intravenously into 5 recipients for a total of 15 recipients/group. For secondary transplantations (noncompetitive situation), cells from 9 primary recipients in each group (control Ab or anti-CD1d treated) were each injected into 3 lethally irradiated B6.BoyJ mice for a total of 27 recipients/group.

Influence of CD1d on hematopoietic stem cells. Comparative engrafting capacities of WT control and CD1d−/− HSCs in lethally irradiated primary mice in a competitive transplantation setting (A,B,D) and a noncompetitive setting (C) without (A-C) and with (D) pretreatment of donor cells with anti-CD1d Ab. All secondary recipient transplantations were done in a noncompetitive setting. Results are expressed as CD45.2+ cell chimerism shown as mean ± SEM with significant differences from WT or untreated cells noted and are based on individual analysis of BM from 3 WT or 3 CD1d−/− mice, each injected intravenously into 5 lethally irradiated recipient B6.BoyJ (CD45.1+) mice along with 5 × 105 nonirradiated B6.BoyJ competitor cells for a total of 15 recipient mice/group (A and B). For secondary transplantations (noncompetitive situation), cells from 9 primary recipients of each group (WT or CD1d−/−) were each injected into 3 lethally irradiated B6.BoyJ mice for a total of 27 recipients per group (A and B). For panel C, 5 × 105 WT or CD1d−/− cells were transplanted as noted in panels A and B in primary B6.BoyJ recipients and secondary transplantations. For panel D, results of CD45.2+ cell chimerism (mean ± SEM) are shown with significant differences noted compared with isotype control Ab–treated cells. 10 × 106 CD45.2+ BM cells were treated with Ab for 30 minutes at 4°C, washed, and injected intravenously at a 1:1 donor-to-nonirradiated (B6.BoyJ, CD45.1+) competitor cell ratio into lethally irradiated B6.BoyJ mice for engraftment analysis of primary mice. Treated donor cells from 3 mice/group were each transplanted intravenously into 5 recipients for a total of 15 recipients/group. For secondary transplantations (noncompetitive situation), cells from 9 primary recipients in each group (control Ab or anti-CD1d treated) were each injected into 3 lethally irradiated B6.BoyJ mice for a total of 27 recipients/group.

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